Neurogenic Bowel Dysfunction and Management
The colon and anorectum are innervated by the sympathetic and parasympathetic autonomic nervous system with somatic innervation to the external sphincter as shown in Figure 1. Disrupted autonomic control of the gastrointestinal (GI) tract is one of the primary causes for neurogenic bowel dysfunction, leading to delayed gastric emptying (Leduc et al. 2002; Gondim et al. 2001; Menter et al. 1997; Rajendran et al. 1992; Fealey et al. 1984) and poor colonic motility (Lynch & Frizelle 2006; Fajardo et al. 2003). This results in prolonged bowel transit time (Brading & Ramalingam 2006; Krogh et al. 2000; Stone et al. 1990a; Lynch et al. 2001), constipation (Faaborg et al. 2008; Finnerup et al. 2008; Lynch et al. 2000), and postprandial (after eating a meal) abdominal distension (Stone et al. 1990a). Left unmanaged, people with neurogenic bowel dysfunction will experience profound constipation and fecal impaction as effective spontaneous evacuation does not occur. In addition, lost or impaired anorectal sensation and loss of somatic voluntary motor control of the external sphincter can lead to unpredictable fecal incontinence. The neurogenic changes are compounded by reduced mobility, polypharmacy, and poor dietary intake.
The gastrointestinal tract has an enteric nervous system divided into the submucosal (Meissner’s) and myenteric (Auerbach’s) plexuses. The enteric system controls gut secretions, blood flow, and muscular activity giving the colon its inherent ability to produce peristalsis. While the autonomic and somatic neural input is disrupted in SCI, the enteric system remains intact.
There are two general patterns in the clinical presentation of bowel dysfunction: injury above the conus medullaris results in upper motor neuron (UMN) bowel syndrome while injury of either the cell bodies within the sacral reflex centre of the conus medullaris or damage to the nerve roots of the cauda equina results in lower motor neuron (LMN) bowel syndrome (Singal et al. 2006; Stiens et al. 1997).
The UMN bowel, or hyperreflexic bowel, is characterized by increased colonic wall and anal tone. Voluntary (cortical) control of the external anal sphincter is lost or impaired and the sphincter remains tight, thereby promoting retention of stool; however, fecal incontinence can and does occur. Although there is loss of supraspinal control, the nerve connections between the spinal cord and the colon remain intact; therefore, there is preserved reflex coordination and stool propulsion. The UMN syndrome is typically associated with constipation and fecal retention at least in part due to external anal sphincter overactivity (Stiens et al. 1997). Stool evacuation in these individuals occurs in response to stimulation of reflex activity, such as presence of feces in the rectum, a suppository, enema, or digital rectal stimulation.
The LMN bowel, or areflexic bowel, is characterized by the loss of centrally-mediated (spinal cord) peristalsis and loss of reflex activity, resulting in slow stool propulsion and impaired reflex stool evacuation. A segmental colonic peristalsis occurs only due to the activity of the enteric nervous system, which is slower and less efficient than the centrally-mediated peristalsis. The result is increased bowel transit times with the production of drier and round-shaped stool. LMN bowel syndrome is commonly associated with constipation and a significant risk of incontinence due to the atonic external anal sphincter and lack of control over the puborecatlis and levator ani muscles; coordinated actions of these striated muscles are important in maintaining continence.
Completeness of injury also has a significant impact on bowel function in people with SCI. Those with an incomplete injury may retain some sensation of rectal fullness and some ability to control evacuation. However, residual rectal sensation may be abnormal and motor control impaired, resulting in fecal urgency or constipation due to disordered defecation reflexes. There are always exceptions to how bowel dysfunction manifests in people with SCI, so careful assessment and a rectal examination are necessary.
To achieve fecal continence and avoid constipation, management of NBD depends upon regular and frequent pre-emptive interventions to empty the bowel at a planned time and frequency. A strict routine using dietary manipulation, rectal stimulants, oral laxatives, and/or physical interventions such as abdominal massage, digital rectal stimulation and manual evacuation of stool is required to establish control over this profoundly important bodily function. Such multifaceted programs are the most used programs for bowel management after SCI (Coggrave et al. 2009) but evidence to support these programs is lacking and much trial and error is involved in development of an effective bowel routine for each person.
Common GI problems reported by up to 41% of people with SCI include abdominal pain and bloating, hemorrhoids, and rectal prolapse (Correa & Rotter 2000). Prolonged bowel evacuation is also common, particularly in people with chronic injuries (Coggrave et al. 2009; Kirk et al. 1997; Lynch et al. 2000); this is as disabling as ineffective management and is associated with anxiety (Glickman & Kamm 1996). The prevalence of chronic GI symptoms increases with time after injury, suggesting that these problems are acquired and potentially preventable (Rajendran et al. 1992).
Autonomic dysreflexia (AD) is a disorder in which people with SCI above the 6th thoracic vertebra (T6) are at risk and is characterized by an abnormal reaction to stimuli below the level of the SCI, resulting in a massive rise in blood pressure that can lead to adverse events including brain hemorrhage and even death. Bowel dysfunction is the second most common cause of AD (Furusawa et al. 2007; Cosman & Vu 2005). Other dangerous complications, though much rarer than AD, like sigmoid volvulus, intestinal obstruction, perianal abscess, and stercoral perforation may also develop (Banwell et al. 1993).
It is important to emphasize that each patient with SCI is unique and that individual bowel programs need to be person-specific. The program will reflect not just residual bowel function and functional abilities but also the person’s goals, lifestyle, and social circumstances. The effectiveness of a bowel program (how well they maintain continence, complete evaculation within a timely manner, etc.) should be re-evaluated regularly and modified as needed.
